The function of the hippocampal formation, a brain structure vital for memory, declines in later life, and in humans the dominant causes are Alzheimer's disease (AD) and the aging process itself1. The hippocampal formation is circuit that is made up molecularly distinct subregions2 and this molecular anatomy accounts for why hippocampal subregions are differentially vulnerable to pathogenic mechanisms. Because of circuit properties, dysfunction in one subregion can affect others, and studies have mapped distinct spatiotemporal patterns of dysfunction in the hippocampal circuit that dissociate AD from aging. In AD, these maps have identified the EC as the subregion differentially affected by the disease3-5 while the dentate gyrus and CA3 are relatively preserved3,4,6, a pattern that has been confirmed in vivo by high-resolution variants of fMRI7-9. In contrast, the EC is relatively preserved in aging, which appears to target other subregions instead. A growing number of high-resolution fMRI8-10 and recent cognitive studies11-14 have, in particular, implicated the DG in aging. Furthermore, in contrast to AD, the effect of aging on hippocampal function begins in at a relatively young age and progresses monotonically across the lifespan8-10,15.